ArticleEuropean journal of histochemistry : EJH2013
KiSS1 inhibits growth and invasion of osteosarcoma cells through inhibition of the MAPK pathway.
Article in European journal of histochemistry : EJH, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- The kisspeptin-1 receptor antagonist peptide-234 aggravates uremic cardiomyopathy in a rat model.Scientific reports · 2023Article
- KISS1 in metastatic cancer research and treatment: potential and paradoxes.Cancer metastasis reviews · 2020Review
- Role of the tumor microenvironment in regulating the anti-metastatic effect of KISS1.Clinical & experimental metastasis · 2020Review
- Autocrine production of reproductive axis neuropeptides affects proliferation of canine osteosarcoma in vitro.BMC cancer · 2019Article
- Exploring the key genes and pathways of side population cells in human osteosarcoma using gene expression array analysis.Journal of orthopaedic surgery and research · 2018Article
- Identifying osteosarcoma metastasis associated genes by weighted gene co-expression network analysis (WGCNA).Medicine · 2018Article
- Astrocytes promote progression of breast cancer metastases to the brain via a KISS1-mediated autophagy.Autophagy · 2017Article
- Down-regulation of RPS9 Inhibits Osteosarcoma Cell Growth through Inactivation of MAPK Signaling Pathway.Journal of Cancer · 2017Article
- Recombinant Lactococcus lactis NZ9000 secretes a bioactive kisspeptin that inhibits proliferation and migration of human colon carcinoma HT-29 cells.Microbial cell factories · 2016Article
- Histochemistry in biology and medicine: a message from the citing journals.European journal of histochemistry : EJH · 2015Review
- The Functional Role of PMP22 Gene in the Proliferation and Invasion of Osteosarcoma.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- Impact of Histochemistry on biomedical research: looking through the articles published in a long-established histochemical journal.European journal of histochemistry : EJH · 2014Article
- Histochemistry as an irreplaceable approach for investigating functional cytology and histology.European journal of histochemistry : EJH · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a metastasis suppressor, KiSS1 has been implicated in numerous human cancers. However, recent studies have demonstrated that KiSS1 promotes tumor growth and metastasis in breast cancer, and it is unclear about the expression and function of KiSS1 in human osteosarcoma (OS). The aim of the present study was to investigate the role and molecular mechanisms of KiSS1 in human OS. The expression of KiSS1 was assessed by immunohistochemical assay using a tissue microarray procedure in forty cases of OS tissues. A gain-of-function approach was used to observe the effects of lentiviral vector-mediated overexpression of KiSS1 (Lv-KiSS1) on the biological behaviors including proliferative activities and invasive potential of OS MG-63 cells, indicated by MTT and Transwell assays, respectively. The results showed that the expression of KiSS1 protein in OS tissues was significantly lowered compared to that in adjacent non-cancerous tissues (ANCT) (42.5% vs 70.0%, P=0.023), and had negative correlation with distant metastases of the tumor (P=0.019). Overexpression of KiSS1 inhibited proliferation and invasion of OS cells with the decreased expression of p38 MAPK and matrix metalloproteinase-9 (MMP-9). Taken together, our findings indicate that the decreased expression of KiSS1 is correlated with distant metastasis of OS, and KiSS1 may function as a tumor suppressor in OS cells through inhibition of the MAPK pathway, suggesting that KiSS1 may serve as a potential therapeutic target for the treatment of cancer.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.